Identification of Potential Molecular Mechanisms and Candidate Genes Involved in The Acute Phase of Myocardial Infarction

Yang, YS; Yang, J; Sui, FH; Huo, PF; Yang, HL

Huo, PF (reprint author), Jilin Univ, China Japan Union Hosp, Intens Care Unit, 126 Xiantai St, Changchun 130031, Jilin, Peoples R China.; Yang, HL (reprint author), Jilin Univ, China Japan Union Hosp, Dept Emergency, Changchun, Jilin, Peoples R China.

CELL JOURNAL, 2018; 20 (3): 435

Abstract

Objective: This study used bioinformatics to determine genetic factors involved in progression of acute myocardial infarction (MI). Materials and Methods: In this prospective study, gene expression profile GSE59867 was downloaded from the Gene Expression Omnibus database, which contained 46 normal samples obtained from stable coronary artery disease patients (n=46) who were without history of MI (control) and 390 samples from patients (n=111) who had evolving ST-segment elevation myocardial infarction (STEMI) as the MI group. These samples were divided into 4 groups based on time points. After identification of differentially expressed genes (DEGs), we conducted hierarchical clustering and functional enrichment analysis. Protein interaction and transcriptional regulation among DEGs were analysed. Results: We observed 8 clusters of DEGs that had a peak or a minimum at the t=1 time point according to gene expression levels. Upregulated DEGs showed significant enrichment in the biological process, single-organism cellular process, response to stimulus and stress, and osteoclast differentiation and lysosome. Downregulated DEGs enriched in the T-cell receptor signalling pathway and natural killer cell mediated cytotoxicity. We identified multiple genes, including signal transducer and activator of transcription 3 (STAT3); LCK proto-oncogene, Src family tyrosine kinase (LCK); and FYN proto-oncogene, Src family tyrosine kinase (FYN) from the protein-protein interaction (PPI) network and/or the transcriptional regulatory network. Conclusion: Cytokine-mediated inflammation, lysosome and osteoclast differentiation, and metabolism processes, as well as STAT3 may be involved in the acute phase of MI.

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